The researchers then used a combination of existing United States Food and Drug Administration - approved drugs to target autophagy and
found ovarian cancer cells to be highly sensitive to these drugs in several different mouse cancer models — even among cells resistant to standard chemotherapy.
Not exact matches
Researchers led by Patricia Donahoe and Xiaolong Wei of Massachusetts General Hospital and Harvard Medical School
found that the common chemotherapy agent doxorubicin actually encourages the growth of
ovarian cancer stem
cells.
Chemotherapy drugs designed to kill tumors may actually encourage
ovarian cancer by stimulating the growth of
cells that give rise to the malignancy, a new study
finds.
Working in
cell cultures and mice, researchers at Johns Hopkins have
found that an experimental drug called fostamatinib combined with the chemotherapy drug paclitaxel may overcome
ovarian cancer cells» resistance to paclitaxel.
In order to
find out how and why
ovarian cancer cells grow and take on such lethal characteristics, Dr. Shepherd and his team grow the
cancer cells in 3D structures, called «spheroids» — the same way the
cancer cells grow in patients.
Analyzing white blood
cells from 934 patients and 1,698 healthy controls, they
found BRCA1 methylation among 6.4 % of patients diagnosed with
ovarian cancer, contrasting 4.2 % among controls.
«For example, we
found that highly aggressive
ovarian cancer cells are glutamine - dependent, and in our laboratory studies, we showed that depriving such
cells of external sources of glutamine — as some experimental drugs do — was an effective way to kill late - stage
cells.
Their
findings in the study «Phosphoglycerate mutase 1 regulates dNTP pool and promotes homologous recombination repair in
cancer cells,» which has been published in The Journal of
Cell Biology, suggest that this FDA - approved
ovarian cancer medicine has the potential to treat a wider range of
cancer types than currently indicated.
In particular, it has been shown that
cells with other HR repair pathway defects, such as BRCA mutations frequently
found in breast and
ovarian cancer, are sensitive to inhibition of the enzyme PARP, and the PARP inhibitor Olaparib has been approved for treatment of BRCA - mutated
ovarian cancers.
The research team with international collaborators analysed more than 100 patient samples from
ovarian and other
cancer types to discover a distinct population of
cells found in some tumours.
The scientists
found that, at certain concentrations, one of the compounds of the series selectively killed human
ovarian cancer cells without harming healthy
cells.
For the new study, described in the October 23rd issue of Nature Communications, scientists at the Johns Hopkins Kimmel
Cancer Center and Dana Farber Cancer Institute in Boston collected tissue samples containing normal cells, ovarian cancers, metastases that had spread elsewhere, and small cancers found in the fallopian tubes, which included single cell layers of cancer called «p53 signatures» and serous tubal intraepithelial carcinoma, or STIC le
Cancer Center and Dana Farber
Cancer Institute in Boston collected tissue samples containing normal cells, ovarian cancers, metastases that had spread elsewhere, and small cancers found in the fallopian tubes, which included single cell layers of cancer called «p53 signatures» and serous tubal intraepithelial carcinoma, or STIC le
Cancer Institute in Boston collected tissue samples containing normal
cells,
ovarian cancers, metastases that had spread elsewhere, and small
cancers found in the fallopian tubes, which included single
cell layers of
cancer called «p53 signatures» and serous tubal intraepithelial carcinoma, or STIC le
cancer called «p53 signatures» and serous tubal intraepithelial carcinoma, or STIC lesions.
In earlier research, Barbolina discovered that a fractalkine receptor — a protein
found on the
cell surface — is expressed in the majority of
ovarian cancer cases.
Blocking a protein
found on the surface of
ovarian cancer cells could prevent or reduce the spread of the disease to other organs, according to new research at the University of Illinois at Chicago.
When the researchers tested the circuit in vitro, they
found that it was able to detect
ovarian cancer cells from amongst other noncancerous
ovarian cells and other
cell types.
They
found that tumor
cells with the mutant genes were particularly sensitive to a drug, olaparib, recently approved for the treatment of hereditary
ovarian cancer.
Those
findings are among results of six studies of investigational chimeric antigen receptor (CAR) T
cells for both adult and pediatric leukemias, adult lymphomas, and
ovarian cancer which will be presented during the 2016 American Society of Clinical Oncology Annual Meeting.
The team
found evidence of the process in several other
cell types, including breast,
ovarian, umbilical cord, and kidney
cancer cells.
In a May 2014 study, Nagrath and colleagues
found that highly aggressive
ovarian cancer cells were glutamine - dependent and that depriving the
cells of external sources of glutamine — as some experimental drugs do — was an effective way to kill late - stage
ovarian cancer cells in the lab.
Liron Bar - Peled and Lynne Chantranupong, who are both authors of the Science article and graduate students in Sabatini's lab,
found that GATOR1 itself is mutated in several
cancers, including glioblastomas and
ovarian cancers, and that
cancer cells with these mutations are also highly sensitive to treatment with rapamycin.
In this video Dr. Odunsi discusses a new study that
found that higher T -
cell diversity in
ovarian cancer is associated with poor overall survival.
The FDA - approved antihelminthic drug, pyrvinium pamoate (PPAM), was
found in a screening for compounds that promoted β - catenin turnover and, thereby, inhibiting Wnt signaling in
ovarian and other
cancer cells (Table 1)[51, 56].
The good news is that if markers for these tubal
cells can be
found, then blood tests, advanced Pap smears, or direct tests on tubal tissue might spot
ovarian cancer earlier, the study authors said.